Microbiology: Current Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Editorial - Microbiology: Current Research (2025) Volume 9, Issue 3

Membrane Trafficking in Host-Pathogen Interactions: A Tug-of-War for Cellular Control

Sachi Anand Patil *

Department of Microbiology, McGill University, Canada

*Corresponding Author:
Sachi Anand Patil
Department of Microbiology, McGill University, Canada
E-mail: sachipatil@gmail.com

Received: 04-Apr-2025, Manuscript No. AAMCR-25-171312; Editor assigned: 05-Apr-2025, PreQC No. AAMCR-25-171312(PQ); Reviewed: 19-Apr-2025, QC No. AAMCR-25-171312; Revised: 23-Apr-2025, Manuscript No. AAMCR-25-171312(R); Published: 30-Apr-2025, DOI:10.35841/AAMCR-9.3.273

Citation: Patil S. A. Membrane trafficking in host-pathogen interactions: A tug-of-war for cellular control. J Micro Bio Curr Res. 2025;9(3):273

Visit for more related articles at Microbiology: Current Research

Introduction

Membrane trafficking is a fundamental cellular process that governs the movement of proteins, lipids, and other macromolecules within and between organelles. It ensures proper cellular organization, signaling, and homeostasis. However, during host-pathogen interactions, this tightly regulated system becomes a battleground. Pathogens—from viruses to bacteria and fungi—have evolved sophisticated strategies to hijack host membrane trafficking pathways, manipulating vesicle transport, organelle dynamics, and immune signaling to promote infection. This tug-of-war for cellular control has profound implications for immunity, pathogenesis, and therapeutic development [1].

Membrane trafficking encompasses two primary pathways: endocytosis and exocytosis. Endocytosis involves the internalization of extracellular materials and plasma membrane components into endosomes, while exocytosis exports cargo from the Golgi apparatus to the plasma membrane or extracellular space. These processes rely on transport vesicles coated with proteins such as clathrin, COPI, and COPII, which mediate vesicle budding, cargo selection, and fusion with target membranes [2].

In addition to these canonical pathways, cells utilize autophagy—a degradation and recycling process involving double-membrane autophagosomes—and phagocytosis, which engulfs large particles including pathogens. Together, these trafficking systems maintain cellular integrity and respond to environmental cues. Pathogens exploit membrane trafficking to gain entry, avoid degradation, and establish replicative niches. Their strategies include: Many pathogens secrete effectors that target host trafficking machinery. For example, bacterial type III secretion systems inject proteins that interfere with vesicle formation and fusion. Viruses like influenza and SARS-CoV-2 use clathrin-mediated endocytosis to enter host cells, while others exploit macropinocytosis or caveolae-dependent pathways [3].

Some pathogens, such as Mycobacterium tuberculosis, block autophagosome maturation to avoid degradation, while others redirect autophagy to support their replication. Intracellular pathogens like Salmonella and Legionella remodel host endosomes and Golgi-derived vesicles to form pathogen-containing vacuoles (PCVs), shielding themselves from immune detection. These receptors detect pathogen-associated molecular patterns (PAMPs) and are trafficked to the plasma membrane or endosomes to initiate signaling. Exocytosis delivers cytokines, chemokines, and antimicrobial peptides to infection sites [4].

The interplay between host and pathogen trafficking systems creates feedback loops that influence infection outcomes. For example:  In plants, detection of effector-mediated trafficking disruption activates robust immune responses. Host cells may reprogram trafficking to isolate pathogens or repair damage, while pathogens counteract with further manipulation. Trafficking of immune receptors and signaling molecules amplifies defense responses, but pathogens may dampen these signals by rerouting vesicles.  Autophagy targets intracellular pathogens for lysosomal degradation, a process known as xenophagy. Membrane trafficking contributes to the execution of apoptosis and pyroptosis, limiting pathogen spread. In plants, membrane trafficking is equally critical in host-pathogen interactions. Pathogens secrete effectors that target vesicle trafficking to suppress immunity. For instance, oomycete and fungal effectors interfere with exocyst complexes and Rab GTPases, disrupting the delivery of immune receptors and defense molecules. Plants respond by redirecting vesicle traffic to infection sites, enhancing secretion of cell wall reinforcements and antimicrobial compounds. Autophagy also plays a role in programmed cell death and immune signaling [5].

Conclusion

Membrane trafficking is a dynamic and multifaceted battleground in host-pathogen interactions. Pathogens deploy intricate strategies to hijack vesicle transport, while hosts mobilize trafficking pathways to detect, respond to, and eliminate invaders. This tug-of-war shapes infection outcomes and offers critical insights into cellular control mechanisms. As research advances, targeting trafficking pathways may yield novel strategies to combat infectious diseases and enhance immune resilience.

References

  1. Gibson GR, Hutkins R, Sanders ME. Expert consensus document: The International Scientific Association for.

    2. Google Scholar

  2. Swanson KS, Gibson GR, Hutkins R. The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of synbiotics. Nat Rev Gastroenterol Hepatol. 2020;17(11):687-701.

    3. Indexed at, Google Scholar

  3. Pineiro M, Stanton C. Probiotic Bacteria: Legislative Framework—Requirements to Evidence Basis1. J Nutr. 2007;137(3):850S-3S.

    4. Indexed at, Google Scholar, Cross Ref

  4. Azad MB, Coneys JG, Kozyrskyj AL. Probiotic supplementation during pregnancy or infancy for the prevention of asthma and wheeze: systematic review and meta-analysis. BMJ. 2013;347.

    5. Indexed at, Google Scholar, Cross Ref

  5. Sonnenburg ED, Sonnenburg JL. The ancestral and industrialized gut microbiota and implications for human health. Nat Rev Microbiol. 2019;17(6):383-90.

    6. Indexed at, Google Scholar, Cross Ref

  6. Marco ML, Heeney D, Binda S. Health benefits of fermented foods: microbiota and beyond. Curr Opin Biotechnol. 2017;44:94-102.

    7. Indexed at, Google Scholar, Cross Ref

  7. Derrien M, van Hylckama Vlieg JE. Fate, activity, and impact of ingested bacteria within the human gut microbiota. Trends Microbiol. 2015;23(6):354-66.

    8. Indexed at, Google Scholar, Cross Ref

  8. Ford AC, Quigley EM, Lacy BE. Efficacy of prebiotics, probiotics, and synbiotics in irritable bowel syndrome and chronic idiopathic constipation: systematic review and meta-analysis. ACG. 2014;109(10):1547-61.

    9. Indexed at, Google Scholar, Cross Ref

  9. Cryan JF, O'Riordan KJ, Cowan CS. The microbiota-gut-brain axis. Physiol Rev. 2019.

    10. Indexed at, Google Scholar, Cross Ref

  10. Slavin J. Fiber and prebiotics: mechanisms and health benefits. Nutrients. 2013;5(4):1417-35.

    11. Indexed at, Google Scholar, Cross Ref

Get the App